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Updated: Jul 4, 2025

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
Valproic acid regulates the miR-155/Jarid2 axis by affecting miR-155 promoter methylation in glioma
Ruixuan Wang1, Yanhong Chen2, Weilu Kuang1
1Department of Oncology, Xiangya Hospital, Central South University, Changsha 410008, China.
Abstract:
The most frequent primary brain tumor in adults is glioma, yet no effective curative treatments are currently available. Our previous study demonstrated the enhancing effects of JARID2 on glioma sensitivity to TMZ treatment. In this study, miR-155 is predicted to target JARID2. miR-155 is overexpressed in clinical glioma specimens and cell lines. miR-155 overexpression in glioma cells enhances cell viability and represses cell apoptosis. Through targeting, miR-155 inhibits JARID2 expression. miR-155 inhibition inhibits glioma cell viability and enhances cell apoptosis, whereas JARID2 knockdown enhances cell viability and inhibits cell apoptosis; JARID2 knockdown partially reverses miR-155 inhibition effects on glioma phenotypes. miR-155 inhibition reduces but knockdown of JARID2 promotes the tumor formation ability of glioma cells in vivo. Valproic acid (VPA) upregulates JARID2 expression, inhibits glioma cell viability and enhances cell apoptosis. VPA downregulates the expression level of miR-155 by increasing the methylation level of the miR-155 promoter, suggesting that the miR-155/JARID2 axis is implicated in VPA inhibition of glioma cell viability and enhancement of glioma cell apoptosis. This study demonstrates a new mechanism of VPA treatment of gliomas by affecting the miR-155/JARID2 axis, which could be regarded as a new strategy for the prevention and treatment of glioma.
Insights
Valproic acid (VPA) impacts glioma treatment by modulating the miR-155/JARID2 axis. VPA upregulates JARID2 and downregulates miR-155, inhibiting glioma cell viability and promoting apoptosis.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Epigenetics
Background:
- Glioma is the most common adult primary brain tumor with limited curative options.
- JARID2 enhances glioma sensitivity to temozolomide (TMZ) treatment.
- MicroRNA-155 (miR-155) is overexpressed in glioma and promotes cell viability while inhibiting apoptosis.
Purpose of the Study:
- To investigate the role of miR-155 in glioma.
- To elucidate the regulatory relationship between miR-155 and JARID2.
- To explore the therapeutic potential of targeting the miR-155/JARID2 axis in glioma.
Main Methods:
- Bioinformatic prediction and experimental validation of miR-155 targeting JARID2.
- Analysis of miR-155 and JARID2 expression in clinical glioma specimens and cell lines.
- In vitro assays assessing cell viability, apoptosis, and in vivo tumor formation.
- Investigation of Valproic acid (VPA) effects on the miR-155/JARID2 axis and glioma phenotypes.
Main Results:
- miR-155 targets and inhibits JARID2 expression in glioma cells.
- miR-155 overexpression enhances glioma cell viability and represses apoptosis.
- miR-155 inhibition decreases glioma cell viability and enhances apoptosis, an effect partially reversed by JARID2 knockdown.
- VPA upregulates JARID2, downregulates miR-155 via promoter methylation, inhibits glioma cell viability, and enhances apoptosis.
Conclusions:
- The miR-155/JARID2 axis plays a critical role in glioma progression.
- Targeting this axis represents a potential therapeutic strategy for glioma.
- VPA exerts anti-glioma effects by modulating the miR-155/JARID2 pathway.
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